Acrylamide is formed during processing of food at high temperature and is documented as a well-known neurotoxic, carcinogenic and has many adverse effects on human health. Therefore, it is the need of hour to reduce the detrimental effect of acrylamide. In the present sub-chronic study 18 adult Wistar rats were randomly divided into three groups. These groups were normal saline, toxicant, and toxicant (19.13 mg/kg) + therapy (20 mg/kg). Our result showed all the sign and symptoms of acrylamide toxicity which include reduction in the body weight, hind limb splaying, hair loss and skin irritation. A significant alteration in the hematological parameters and sharp enhancement in AST, ALT, ALP, LDH, GGT, urea, uric acid and triglycerides was recorded. Activity of acetylcholinesterase significantly reduced in brain after acrylamide administration. Acrylamide exposure resulted into increased mean DNA damage and tail length in liver, kidney and brain as compared to normal evident by COMET assay. Our biochemical findings were reinforced by histological observation. Treatment with caffeic acid restored tissue and serological indices accompanying towards normal.
Background: Tephrosia purpurea (TP), commonly known as wild indigo, is traditionally used in treatment of splenomegaly. It is an important ingredient of various Ayurvedic medicines used in treatment of liver diseases. Objectives: Thus, the study was undertaken to investigate the hepatoprotective efficacy of ethanolic extract of TP against Aflatoxin B1 (AFB1) induced liver injury. Materials and Methods: The ethanolic extract of TP was prepared by Soxhlet extraction method. Presence of polyphenols and antioxidant potential were assessed. The antiproliferative activity of extract was tested on HepG2 cells using MTT assay. For in vivo studies female Wistar rats were randomly divided into 6 groups with 6 animals in each. The entire regime was of 33 days. AFB1 was administered at 200 µg/kg dose and TP was administered at three different doses (100, 200 and 300 mg/kg). 24 hr after last treatment the animals were euthanised and liver and blood samples were collected. Results: 45.77± 2.53 µg/ ml IC 50 of extract was seen on HepG2 cells. A significant elevation in serum transaminases, triglycerides (TG) and LPO was seen after AFB1 intoxication. Whereas decline in activities of GSH, SOD, CAT, G6Pase and ATPase were observed. Treatment with different doses of TP restored its activities towards normal indices. Maximum recovery was seen with 300 mg/kg dose of TP. Conclusion: It may be concluded that TP possess hepatoprotective efficacy against AFB1 induced oxidative injury and it may prove to be of clinical use after further studies.
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